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    InvivoChem Cat #: V0299
    CAS #: 927822-86-4 Purity ≥98%

    Description: KC7F2 is a novel and potent HIF-1 (hypoxia inducible factor-1) pathway inhibitor with potential anticancer activity. KC7F2 is cytotoxic agent to a variety of cancer cell lines with an IC50 value of 15-25 µM. KC7F2 markedly inhibited HIF-mediated transcription in cells derived from different tumor types, including glioma, breast, and prostate cancers, and exhibited enhanced cytotoxicity under hypoxia. KC7F2 prevented the activation of HIF-target genes such as carbonic anhydrase IX, matrix metalloproteinase 2, endothelin 1, and enolase 1.

    References:Clin Cancer Res. 2009 Oct 1;15(19):6128-36; Neuropharmacology. 2014 Feb;77:428-40; Synapse. 2014 Sep;68(9):402-9.

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    Molecular Weight (MW)




    CAS No.



    -20℃ for 3 years in powder form

    -80℃ for 2 years in solvent

    Solubility (In vitro)

    DMSO: 100 mg/mL (175.3 mM)

    Water:<1 mg/mL 

    Ethanol:<1 mg/mL

    Solubility (In vivo)

    Chemical Name: N,N'-(disulfanediylbis(ethane-2,1-diyl))bis(2,5-dichlorobenzenesulfonamide)


    InChi Code: InChI=1S/C16H16Cl4N2O4S4/c17-11-1-3-13(19)15(9-11)29(23,24)21-5-7-27-28-8-6-22-30(25,26)16-10-12(18)2-4-14(16)20/h1-4,9-10,21-22H,5-8H2

    SMILES Code: ClC1=C(S(NCCSSCCNS(C2=C(Cl)C=CC(Cl)=C2)(=O)=O)(=O)=O)C=C(Cl)C=C1


    KC-7F2; KC 7F2; KC7F2

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    In Vitro

    In vitro activity: KC7F2 inhibits HRE-driven transcription and decreases HIF-1α protein levels in LN229-HRE-AP cells. KC7F2 shows a dose-response cytotoxicity with IC50 of approximately 15 to 25 μM in cancer cells MCF7, LNZ308, A549, U251MG, and LN229. In D54MG glioma cells, KC7F2 inhibits colony formation, especially under hypoxia. In hypoxic microglial cultures, KC7F2 downregulates the expression of TfR and DMT, and reduces the HIF-1α mediated iron accumulation.


    Kinase Assay: Cells are incubated at 37°C in a humidified atmosphere containing 5% CO2 and 21% O2 (normoxia) or 1% O2 (hypoxia) in a hypoxia workstation. The LN229-HRE-AP reporter cell line for HIF transcriptional activity is created by stably transfecting LN229 cells with the pACN188 plasmid, which contains an alkaline phosphatase gene driven by six HREs derived from the VEGF gene.


    Cell Assay: Cells (Human dermal microvascular endothelial cells and mouse neurons; MCF7, LNZ308, A549, U251MG, and LN229 cell lines) are seeded onto 96-well plates (4 × 103/well) and cultured under normoxic (21% O2) and hypoxic (1% O2) conditions with different concentrations of KC7F2 for 72 h or treated for various times with 20 μM KC7F2. For proliferation analysis, cells are fixed with 50% trichloroacetic acid for 1 h at 4°C, followed by staining with 0.4% sulforhodamine B dissolved in 1% acetic acid for 30 min at room temperature. Plates are washed five times with 1% acetic acid to remove unbound dye. Bound dye is dissolved by adding 10 mM unbuffered Tris base. Cell proliferation is calculated by measuring OD values at 564 nm using a spectrophotometer.

    In Vivo

    KC7F2 significantly reduces the latent period in the pentylenetetrazole kindling rat model and increases the rate of spontaneous recurrent seizures during the chronic stage in the lithium-pilocarpine rat model.

    Animal model

    In a rat epilepsy model, KC7F2 significantly shortened the latent period in the PTZ kindling model and increased the rate of spontaneous recurrent seizures during the chronic stage in the lithium-pilocarpine model

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    Clin Cancer Res. 2009 Oct 1;15(19):6128-36; Neuropharmacology. 2014 Feb;77:428-40; Synapse. 2014 Sep;68(9):402-9.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    KC7F2 inhibits HRE-driven transcription. Clin Cancer Res. 2009 Oct 1;15(19):6128-36.


    Cytotoxicity analysis in response to KC7F2 treatment. Clin Cancer Res. 2009 Oct 1;15(19):6128-36.


    KC7F2 reduces the protein levels of HIF-1α in cancer cell lines of different tissue origin and genetic background. Clin Cancer Res. 2009 Oct 1;15(19):6128-36.


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